A spike in serum creatinine and/or a decrease in urine output have typically been used to diagnose AKI. From the Risk, Injury, Failure, Loss, End-stage (RIFLE) criteria in 2004 to the AKI Network (AKIN) categorization in 2007 [4, 5], the definition has developed. Both were integrated in 2012, resulting in the KDIGO (Kidney Disease Improving Global Outcomes) classification.
AKI is defined as a spike in serum creatinine of 0.3 mg/dl (26.5 mol/l) or more in 48 hours or a rise of at least 1.5-fold from baseline in 7 days (Table 1). The maximum change in serum creatinine or urine output determines the stage of AKI. The relevance of these criteria was validated in a recent research of more than 32,000 critically sick patients, which found that patients who satisfied both criteria for AKI and had these anomalies for more than 3 days had the highest short- and long-term risk of mortality or RRT.
A link between AKI stages and short- and long-term outcomes has been demonstrated in several investigations in a variety of patient populations [8–13]. Serum creatinine and urine output, on the other hand, are excretory function markers and do not reveal anything about the kidney's other activities, such as metabolic, endocrine, or immunological processes. They're also not kidney-specific and must be understood in the context of the patient's medical history. Some people satisfy the AKI definition but do not have AKI, whereas others have obvious indications of renal impairment but do not meet the AKI creatinine or urine requirements.
Acute Kidney Injury (AKI): Diagnostic approach
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